Cytokines sing the blues: inflammation and the pathogenesis of depression

• Authors: Charles L. Raison, Emory University; Lucile Capuron, Emory University; Andrew H Miller, Emory University
• Journal Title: Trends in Immunology
• Volume: Volume 27, Number 1
• Publisher: Elsevier (Cell Press) | 2006-01, Pages 24-31
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1016/j.it.2005.11.006
• Subjects: Psychology, Physiological

Abstract

Increasing amounts of data suggest that inflammatory responses have an important role in the pathophysiology of depression. Depressed patients have been found to have higher levels of proinflammatory cytokines, acute phase proteins, chemokines and cellular adhesion molecules. In addition, therapeutic administration of the cytokine interferon-α leads to depression in up to 50% of patients. Moreover, proinflammatory cytokines have been found to interact with many of the pathophysiological domains that characterize depression, including neurotransmitter metabolism, neuroendocrine function, synaptic plasticity and behavior. Stress, which can precipitate depression, can also promote inflammatory responses through effects on sympathetic and parasympathetic nervous system pathways. Finally, depression might be a behavioral byproduct of early adaptive advantages conferred by genes that promote inflammation. These findings suggest that targeting proinflammatory cytokines and their signaling pathways might represent a novel strategy to treat depression.